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doi: 10.1007/s00701-021-05038-0

However, Galloway and McLellan found that while an AP-1 site at 340 of human GCLM modulated basal expression of GCLM, neither the AP-1 site nor the ARE/EpRE site at 302 was involved in mediating the up-regulation of GCLM by TBH (Galloway et al., 1998)

Furthermore, given the abundance of CB1 receptors in the brain, understanding the consequences of long-term cannabinoid receptor inhibition is crucial before introducing new agents

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